Evidence map›Paper›PMID 20726883›Full record

ArticleThe European journal of neuroscience2010

Alcohol consumption enhances antiretroviral painful peripheral neuropathy by mitochondrial mechanisms.

Luiz F Ferrari, Jon D Levine

Abstract read
In one paragraph

Article in The European journal of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Drug-Induced Peripheral Neuropathy: A Narrative Review.Current clinical pharmacology · 2020
    Review
  11. Article
  12. Antiretroviral drug-S for a possible HIV elimination.International journal of physiology, pathophysiology and pharmacology · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Luiz F FerrariNIH Pain Center (UCSF), Division of Neuroscience and Biomedical Sciences Program, University of California at San Francisco, San Francisco, CA 94143, USA.
Jon D Levine
University of California, San Francisco · US

Funding

Receptors and Second Messengers for Pain and AnalgesiaP01NS053709 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEVINE, JON DAVID · 2007 to 2011
$5.0M
Mechanisms of Interactions of Alcohol Abuse HIV NeuropathogenesisR01AA017384 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEVINE, JON DAVID · 2008 to 2012
$1.7M
NIAAA NIH HHS R01 AA017384NINDS NIH HHS P01 NS053709
6 · The paper itself

Abstract

A major dose-limiting side effect of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) chemotherapies, such as the nucleoside reverse transcriptase inhibitors (NRTIs), is a small-fiber painful peripheral neuropathy, mediated by its mitochondrial toxicity. Co-morbid conditions may also contribute to this dose-limiting effect of HIV/AIDS treatment. Alcohol abuse, which alone also produces painful neuropathy, is one of the most important co-morbid risk factors for peripheral neuropathy in patients with HIV/AIDS. Despite the prevalence of this problem and its serious impact on the quality of life and continued therapy in HIV/AIDS patients, the mechanisms by which alcohol abuse exacerbates highly active antiretroviral therapy (HAART)-induced neuropathic pain has not been demonstrated. In this study, performed in rats, we investigated the cellular mechanism by which consumed alcohol impacts antiretroviral-induced neuropathic pain. NRTI 2',3'-dideoxycytidine (ddC; 50 mg/kg) neuropathy was mitochondrial-dependent and PKCε-independent, and alcohol-induced painful neuropathy was PKCε-dependent and mitochondrial-independent. At low doses, ddC (5 mg/kg) and alcohol (6.5% ethanol diet for 1 week), which alone do not affect nociception, together produce profound mechanical hyperalgesia. This hyperalgesia is mitochondrial-dependent but PKCε-independent. These experiments, which provide the first model for studying the impact of co-morbidity in painful neuropathy, support the clinical impression that alcohol consumption enhances HIV/AIDS therapy neuropathy, and provide evidence for a role of mitochondrial mechanisms underlying this interaction.

Indexed as

Alcoholic NeuropathyAnimalsAnti-HIV AgentsDisease Models, AnimalDrug InteractionsElectron Transport Chain Complex ProteinsEthanolHyperalgesiaMaleMitochondriaOligodeoxyribonucleotides, AntisensePeripheral Nervous System DiseasesProtein Kinase C-epsilonRatsRats, Sprague-DawleyZalcitabineAnti-HIV AgentsElectron Transport Chain Complex ProteinsEthanolOligodeoxyribonucleotides, AntisenseProtein Kinase C-epsilonZalcitabine

Identifiers

PMID20726883
PMCPMC2974761
OpenAlexW1570620904

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.